Annexin A1 and the Resolution of Inflammation: Modulation of Neutrophil Recruitment, Apoptosis, and Clearance

Sugimoto, Michelle A.; Vago, Juliana P.; Teixeira, Mauro Martins; Sousa, Lirlândia P.

doi:10.1155/2016/8239258

Cited by 292 publications

(238 citation statements)

References 111 publications

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“…Strikingly, and supporting earlier in vivo studies with recombinant AnxA1 tools (Perretti and Dalli, 2009;Sugimoto et al, 2016), AnxA1 -/-mice displayed a boosted immune response. This was characterized by an increased leucocyte migratory behavior and Croxtall et al, 2003;Hannon et al, 2003;Damazo et al, 2011;Drechsler et al, 2015reviewed in D'Acquisto et al, 2008Perretti and D'Acquisto, 2009;Perretti and Dalli, 2009;Gavins and Hickey, 2012;Yang et al, 2013a;Sugimoto et al, 2016Nair et al, 2015Yang et al 2013breviewed in D'Acquisto et al, 2008Perretti and D'Acquisto, 2009;Perretti and Dalli, 2009;Gavins and Hickey, 2012;Yang et al, 2013a;Sugimoto et al, 2016 Wound (Hannon et al, 2003). Altogether, this prominent extracellular AnxA1 activity suggested the existence of an AnxA1 receptor.…”

Section: Anxa1 Ko Micesupporting

confidence: 82%

“…It would go beyond the scope of this review to summarize all this research. Thus we point the reader to excellent reviews with comprehensive lists of in vivo investigations using AnxA1 -/-mice or AnxA1-derived peptides from Perretti and colleagues (D'Acquisto et al, 2008;Perretti and D'Acquisto, 2009;Perretti and Dalli 2009), and more recently from others (Gavins and Hickey, 2012;Yang et al, 2013a;Sugimoto et al, 2016). Overall these studies have provided an enormous depth of information on the variety of AnxA1/FPR2-mediated immunological consequences in various cell types driving the innate immune response.…”

Section: Anxa1 Ko Micementioning

confidence: 96%

“…To date, administration of the AnxA1 derived N-terminal Ac2-26 peptide is the most common approach (D'Acquisto et al, 2008;Perretti and D'Acquisto, 2009;Perretti and Dalli, 2009;Gavins and Hickey, 2012;Yang et al, 2013a;Locatelli et al, 2014;Sugimoto et al, 2016). Overall, exogenous administration of AnxA1 or AnxA1-derived peptides are effective to limit or resolve inflammation in a large range of disease models in rodents, including stroke, myocardial ischemia, non-alcoholic steatohepatitis, rheumatoid arthritis, multiple sclerosis, colitis and asthma.…”

Section: Anxa1 Ko Micementioning

confidence: 99%

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Annexins – insights from knockout mice

Grewal

Wason

Enrich

et al. 2016

Biological Chemistry

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Annexins are a highly conserved protein family that bind to phospholipids in a calcium (Ca 2+ ) -dependent manner. Studies with purified annexins, as well as overexpression and knockdown approaches identified multiple functions predominantly linked to their dynamic and reversible membrane binding behavior. However, most annexins are found at multiple locations and interact with numerous proteins. Furthermore, similar membrane binding characteristics, overlapping localizations and shared interaction partners have complicated identification of their precise functions. To gain insight into annexin function in vivo, mouse models deficient of annexin A1 (AnxA1), A2, A4, A5, A6 and A7 have been generated. Interestingly, with the exception of one study, all mice strains lacking one or even two annexins are viable and develop normally. This suggested redundancy within annexins, but examining these knockout (KO) strains under stress conditions revealed striking phenotypes, identifying underlying mechanisms specific for individual annexins, often supporting Ca 2+ homeostasis and membrane transport as central for annexin biology. Conversely, mice lacking AnxA1 or A2 show extracellular functions relevant in health and disease that appear independent of membrane trafficking or Ca 2+ signaling. This review will summarize the mechanistic insights gained from studies utilizing mouse models lacking members of the annexin family.

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Section: Anxa1 Ko Micesupporting

confidence: 82%

Section: Anxa1 Ko Micementioning

confidence: 96%

Section: Anxa1 Ko Micementioning

confidence: 99%

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Annexins – insights from knockout mice

Grewal

Wason

Enrich

et al. 2016

Biological Chemistry

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“…However, this may not be a problem for R115777 therapy because it induces tumor cell apoptosis and the apoptotic cells or apoptotic bodies are engulfed by macrophages through phagocytosis and the insulin inside the dead cells/bodies will most possibly be degraded by the lysosomal enzymes of the macrophages [47][48][49][50]. In addition, if the drug could be used clinically, the patients should be administered with glucose or other medications to prevent any possible hypoglycemia.…”

Section: Discussionmentioning

confidence: 99%

A farnesyl transferase inhibitor induces apoptosis of insulinoma pancreatic β cells of mouse

Gao¹,

Fu²,

Liu³

et al. 2018

biomedicalresearch

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This study is to investigate the effect of a Farnesyl Transferase Inhibitor (FTI) R115777 on apoptosis of mouse insulinoma pancreatic β cells. MTT assay was used to investigate the proliferative inhibition of in vitro cultured mouse insulinoma pancreatic β cell lines by a FTI R115777. The morphological changes of the cells were observed using a fluorescence microscope by staining with Hoechst 33258 and propidium iodide after the treatment with FTI R115777. The apoptosis rate of R115777-treated beta-TC-6 cells was detected by flow cytometry. The expressions of caspase-3 and caspase-9 of the R115777-treated beta-TC-6 cells were assayed by spectrophotometry. In addition, the sub-cellular distribution of cytochrome c and the expressions of Bax and Bcl-2 proteins were detected by Western blot. After the treatment with FTI R115777, the proliferation of the mouse insulinoma pancreatic β cell lines was significantly inhibited. Significant apoptosis was observed in the treated beta-TC-6 cells. The effect of R115777 on the apoptosis of beta-TC-6 cells showed time-and dose-dependent manners. The expressions of caspase-3, caspase-9 and Bax in the R115777-treated beta-TC-6 cells increased, while the expression of Bcl-2 decreased. The sub-cellular distribution of cytochrome-c changed, with reduced cytochrome-c in mitochondria and increased cytochrome-c in cytoplasm. FTI R115777 can inhibit the proliferation of mouse insulinoma pancreatic β cell lines, and might induce cell apoptosis through the mitochondrionmediated pathway. R115777 could be further studied as a potential antitumor drug.

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“…Therefore, the ectopic expression of ANXA1 is thought to drive various cancer developments 2,3) . We previously reported that a breast cancer case of positive ANXA1 expression by immunohistochemical (IHC) staining was frequently identified in triple-negative breast cancer (P = 0.007) and was associated with positive venous invasion (P = 0.028) 4) .…”

Section: Introductionmentioning

confidence: 99%

Annexin A1 is upregulated in p53-positive gastric cancer

Saito

Nakano

Kikuchi

et al. 2018

Ann. Cancer Res. Therap.

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Annexin A1 (ANXA1) is a calcium-dependent phospholipid-linked protein that is associated with anti-inflammatory effects, regulation of cellular differentiation, proliferation, and apoptosis. In gastric cancer, ANXA1 is upregulated and has a significant role of gastric tumorigenesis. Although ANXA1 is known to be a p53 target gene, the association between ANXA1 expression and p53 expression is yet to be fully investigated in gastric cancer. We therefore investigated in this study the expressions of ANXA1 and p53 by immunohistochemical (IHC) staining in 231 gastric cancer tumors. ANXA1 expression was positive in 108 cases (46.8%), whereas negative in 123 cases (53.2%). p53 expression was positive in 109 cases (47.2%), but negative in 122 cases (52.8%). The percentage of positive ANXA1 was significantly higher in p53 positive tumors compared with p53 negative tumors (P < 0.001). We next performed IHC staining for ANXA1 and p53 in three human gastric cancer cell lines (MKN28, NUGU4, KATOIII). Positive staining for ANXA1 and p53 was detected in MKN28 cells with TP53 gene mutations. On the other hand, weak positive staining for ANXA1 and positive staining for p53 was found in NUGC4 and KATOIII cells with TP53 wild-type and truncating mutations, respectively. Our results demonstrated that ANXA1 is upregulated in p53-positive gastric cancer. ANXA1 expression may be induced by aberrant p53 protein, providing the possibility that ANXA1 works with the TP53 gene in gastric cancer.

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Annexin A1 and the Resolution of Inflammation: Modulation of Neutrophil Recruitment, Apoptosis, and Clearance

Cited by 292 publications

References 111 publications

Annexins – insights from knockout mice

Annexins – insights from knockout mice

A farnesyl transferase inhibitor induces apoptosis of insulinoma pancreatic β cells of mouse

Annexin A1 is upregulated in p53-positive gastric cancer

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